Continuing Education Activity

Catatonia is a complex and underrecognized neuropsychiatric syndrome that affects patients across the lifespan and arises from psychiatric, medical, neurologic, and autoimmune conditions. The syndrome presents with motor, behavioral, and autonomic abnormalities and may accompany mood disorders, schizophrenia, or general medical illnesses. Despite its potential for rapid deterioration and life-threatening complications such as malignant catatonia, prompt recognition and treatment often lead to recovery. Understanding dysregulation of gamma-aminobutyric acid and glutamate neurotransmission enhances diagnostic precision and therapeutic outcomes. Diagnosis relies on validated assessment tools such as the Bush-Francis Catatonia Rating Scale, and management involves benzodiazepines, electroconvulsive therapy, and emerging agents, including N-methyl-D-aspartate antagonists and ketamine.

Through participation in this activity, clinicians strengthen competence in recognizing, assessing, and managing catatonia using evidence-based approaches. Learners review advances in epidemiology, pathophysiology, and therapeutics, including noninvasive brain stimulation and pharmacologic strategies for refractory cases. The course emphasizes interprofessional collaboration among psychiatrists, neurologists, pediatricians, nurses, and allied clinicians, fostering coordinated assessment, treatment, and monitoring. Enhanced communication within the care team enables early detection, timely intervention, and prevention of complications. 

Objectives:

• Identify the diagnostic features and subtypes of catatonia using diagnostic criteria and validated rating scales.
• Evaluate current and emerging treatment modalities for catatonia, including benzodiazepines, electroconvulsive therapy, N-methyl-D-aspartate receptor antagonists, and noninvasive neuromodulation techniques.
• Interpret recent advances in the understanding of the pathophysiology of catatonia, including neuroimaging findings, neurotransmitter dysfunction, and autoimmune mechanisms, to inform diagnostic accuracy and therapeutic decision-making.
• Collaborate effectively as an interprofessional healthcare team to ensure timely identification, comprehensive assessment, and coordinated management of catatonia, enhancing communication pathways and reducing delays in critical interventions.

Introduction

Leopold Bellack described the derivation of the term catatonia from the Greek roots kata (meaning "down") and tonos (meaning "tension" or "tone").[1] Catatonia was first categorically studied in 1854 by Karl Kahlbaum.[2] Historically, catatonia was considered a subtype of schizophrenia.[3] Catatonia is now understood to be a neuropsychiatric syndrome with diverse etiologies, ranging from primary psychiatric disorders to neurological and medical conditions, characterized by a range of motor, behavioral, and affective abnormalities that can be potentially fatal if untreated.[3][4][5] Recent developments have enhanced our understanding of its epidemiology, pathophysiology, diagnostic criteria, and treatment modalities. Including catatonia as an independent diagnosis in the International Classification of Diseases, 11th Revision, further highlights its clinical significance.[6]

Etiology

Catatonia can present across a broad spectrum of medical, neurologic, and psychiatric conditions and affects individuals of all ages, from children to older adults. Delayed diagnosis increases the risk of complications such as malnutrition, infections, and even death.

Psychiatric Etiologies

Psychiatric diseases are the most common causes of catatonia:

• Mood disorders (eg, major depressive disorder, bipolar disorder): Catatonia frequently occurs during severe mood episodes, particularly in melancholic depression or manic states with psychotic features. Notably, mood disorders account for more cases of catatonia than schizophrenia.[7][8]
• Psychotic disorders (eg, schizophrenia, schizoaffective disorder): Historically linked to schizophrenia, catatonia in this context often features negativism, rigidity, waxy flexibility, and mannerisms. Chronic catatonic schizophrenia is rare, but acute catatonic episodes in schizophrenia are clinically significant and usually respond to benzodiazepines or electroconvulsive therapy.[9]
• Autism spectrum disorder: In both adolescents and adults with autism spectrum disorder, catatonia may manifest as regression, freezing, mutism, or repetitive motor behaviors, often precipitated by stress or changes in routine. Misdiagnosis as worsening autism is common.[10][11]
• Trauma and stress-related disorders: (eg, posttraumatic stress disorder, dissociative stupor): Severe psychological trauma may precipitate catatonic features, particularly immobility and mutism, as part of a dissociative or shutdown response.[12] 

 Neurologic Etiologies

Catatonia may emerge from structural or functional disturbances in the brain:

• Epilepsy (usually in the temporal lobe): Nonconvulsive status epilepticus may mimic catatonia, especially in fluctuating presentations. Electroencephalographic (EEG) studies are essential to exclude seizure as a cause. Postictal catatonia is also documented in both adults and children.[13][14]
• Traumatic brain injury: Catatonia has been reported following moderate to severe traumatic brain injury.[15]
• Stroke and hypoxic-ischemic encephalopathy: Basal ganglia infarcts, hypoxia, or global anoxic injury may produce catatonic features, especially in older adults.[2]
• Delirium and encephalopathy: While traditionally considered mutually exclusive, catatonia and delirium can occur concurrently. Patients (particularly older adults) may alternate between hypoactive delirium and catatonic stupor, particularly in toxic-metabolic states.[16]

Metabolic and Toxic Etiologies

Numerous systemic disturbances can precipitate catatonia, primarily when they affect brain metabolism or neurotransmitter systems:

• Encephalopathy: Encephalopathy is associated with metabolic or infectious causes and can cause catatonia.[6]
• Wilson disease: This disorder of copper metabolism may present with both neurologic and psychiatric symptoms, including catatonia, tremor, dystonia, or Parkinsonism.[17]

Drug-Induced and Withdrawal States

Drug intoxication (eg, cannabis, cocaine) and withdrawal (eg, alcohol, opioids, benzodiazepines) can precipitate catatonia.[6] Intoxication with cannabis or cocaine can cause fluctuating levels of psychomotor behavior rapidly, ranging from mutism and stupor to posturing and agitation.[6]

Autoimmune and Inflammatory Etiologies

Autoimmune encephalitis and related conditions are increasingly recognized as causes of acute catatonia, particularly in younger adults:

• Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis: Anti-NMDA receptor encephalitis can present with catatonia. The autoimmune attack on NMDA receptors disrupts glutamatergic signaling, leading to symptoms such as mutism, posturing, stupor, and rigidity, hallmarks of catatonia. These symptoms often occur alongside psychosis, seizures, and autonomic instability.[18] Anti-NMDA receptor encephalitis accounts for 72% of all autoimmune-related catatonia.[19]
• Other autoimmune encephalitides: Autoimmune antibodies, including anti–leucine–rich glioma-inactivated 1, anti–glutamic acid decarboxylase 65-kilodalton isoform (GAD65), anti-γ-aminobutyric acid (GABAA, GABAB) receptor, anti-dipeptidyl-peptidase-like protein-6, and anti-glycine receptor, can cause catatonia. These antibodies disrupt brain function, leading to catatonic states. Testing for these antibodies should be considered in cases of unexplained catatonia to guide diagnosis and treatment.[19]
• Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections/pediatric acute-onset neuropsychiatric syndrome: Neuropsychiatric disorders following infection in children and adolescents can present with sudden-onset obsessive-compulsive disorder, tics, and neuropsychiatric symptoms, occasionally including catatonia, following infections due to immune-mediated basal ganglia dysfunction.[20]

Epidemiology

Results from recent population-based studies have provided insights into the incidence and prevalence of catatonia. Data from the United Kingdom indicate an incidence of 4.3 episodes per 100,000 person-years and a 1-year prevalence of 4.4 per 100,000 persons. In the United States, the 1-year prevalence of catatonia-related hospitalizations is approximately 5.1 per 100,000 persons.[21]

Pathophysiology

The pathophysiology of catatonia is complex and likely involves dysfunction in multiple neural circuits. Catatonia is best conceptualized as a final common pathway of diverse pathophysiologic insults affecting frontal-subcortical circuits and GABAergic, glutamatergic, and dopaminergic systems. 

Neuroanatomical Findings

Although neurobiological correlates have been identified, it is not clear if these findings are causes or effects of catatonia.

• Basal ganglia dysfunction: Abnormalities in the cortico-striato-thalamo-cortical loops, particularly involving the basal ganglia and frontal cortex, have been implicated in motor symptoms of catatonia.[22]
• GABAergic hypofunction:

  • Reduced GABA activity, particularly in the prefrontal cortex, may contribute to catatonic states. This theory is supported by the efficacy of benzodiazepines, which enhance GABA_A receptor function.[2]
  • Excessive NMDA receptor activation (eg, anti-NMDA receptor encephalitis) can lead to a catatonic syndrome, further linking the disorder to an imbalance between inhibitory and excitatory neurotransmission.[23]
  • NMDA receptor hypofunction has been proposed, particularly in autoimmune-related catatonia, given the overlap with anti-NMDA receptor encephalitis.[23]
• Neuroimaging findings: Generalized cerebral atrophy and nonspecific white matter abnormalities have also been reported.[16][24]

Laboratory Findings 

There are no known biochemical markers for diagnosing catatonia. Laboratory findings such as reduced ceruloplasmin levels indicate an underlying medical cause (eg, Wilson disease). Other laboratory findings, such as elevated creatine kinase levels, indicate complications of catatonia, such as muscle breakdown or rhabdomyolysis.

Dysautonomia and Neuroinflammation 

Cases of catatonia associated with autoimmune encephalitis highlight the role of immune-mediated neural dysfunction.[23] Autoimmune processes, particularly anti-NMDA receptor encephalitis, have been implicated in the pathogenesis of catatonia. Various autoantibodies, including antineuronal nuclear antibody type 1 (Hu), anti-GABA_A receptor, and anti-GAD65, have been documented, although their exact roles remain to be elucidated.[16][24]

History and Physical

Catatonia was previously described as an abrupt and remarkable withdrawal from the senses and the environment in the context of a psychotic or mood disorder.[25] In general, catatonia is characterized by a change in movement and behavior, either increased, decreased, or abnormal, compared to baseline, in the context of intact physical capacity for motor movement.[25] Catatonia is defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, Text Revision, by the presence of 3 or more of 12 psychomotor features:

1. Stupor: Profound unresponsiveness to external stimuli
2. Catalepsy: Passively holding a fixed posture against gravity
3. Waxy flexibility: Slight, even resistance to positioning by examiner
4. Mutism: No, or very little, verbal response (exclude known conditions causing aphasia) 
5. Negativism: Opposition or lack of response to instructions or external stimuli
6. Posturing: Spontaneous and active maintenance of a posture against gravity
7. Mannerism: Odd, circumstantial caricature of normal actions
8. Stereotypy: Repetitive, abnormally frequent, non–goal-directed movements
9. Agitation: Not influenced by external stimuli
10. Grimacing
11. Echolalia: Mimicking another’s speech
12. Echopraxia: Mimicking another’s movements

The onset can be insidious or acute.[6] In the literature, patients described their experience in various ways. Some expressed a complete loss of recollection, while others reported intact awareness but a loss of communication ability.[26] 

Types of Catatonia Presentations

Depending upon the nature of movement disturbance and associated clinical features, 3 primary subtypes of catatonia are identified: akinetic (retarded) catatonia, hyperkinetic (excited) catatonia, and malignant catatonia.[27] Retarded catatonia and excited catatonia may appear concurrently or may transition between one another in no specific order.[28] Either subtype may progress to malignant catatonia, or the malignant form may occur in the absence of retarded or excited catatonia.[28][29]

Akinetic catatonia (retarded catatonia)

This form is characterized by mutism, inhibited movement, posturing, negativism, and staring.[30][31] Postures may be mundane (eg, sitting or standing in the same position for hours) or unusual (eg, head raised above the bed as if on a pillow). Speech, spontaneous movements, and response to voice or noxious stimuli are decreased. Alertness and awareness may vary. In more severe cases, eating and drinking may cease, and stupor and incontinence may occur.[32]

Excited catatonia (hyperkinetic catatonia)

This subtype is characterized by excessive and purposeless motor activity in the upper and lower extremities (hyperkinesis), restlessness, stereotypy (repetitive movements such as pacing or grimacing), impulsivity (sudden, unpredictable agitation), verbigeration (repetitive, meaningless speech), and paradoxical negativism (doing the opposite of what the examiner asks such as sitting when asked to stand).[30][31] Delirium may occur in severe cases, and excessive motor activity may lead to self-injury or harm to others.[33]

Malignant catatonia (life-threatening form)

Catatonia with escalating fever and autonomic instability was historically termed lethal catatonia because of the high mortality rates in the 1960s through 1980s. After 1986, the term was changed to malignant catatonia as mortality rates declined significantly with advances in medical care and interventions.[34][35] This life-threatening condition is characterized by fever (≥38.5 °C [101.3 °F]), autonomic instability (labile or elevated blood pressure, tachycardia, tachypnea, and diaphoresis), delirium, and rigidity, which can progress rapidly.[30][31][36] 

Periodic catatonia

Periodic catatonia is a rare, heritable subtype associated with specific genetic mutations and autosomal dominant inheritance, with a chronic, degenerative course.[37][38] Rolv Gjessing proposed that the disorder was related to a cyclic nitrogen imbalance and proposed treatment with thyroid hormone extract.[34][39] Periodic catatonia currently lacks a nosological definition in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, Text Revision.[40]

Evaluation

While the diagnosis of catatonia is clinical, the British Association for Psychopharmacology released comprehensive guidelines in 2023 that emphasize an interdisciplinary approach to diagnosis and management. Key recommendations include a thorough evaluation for underlying medical or neurologic conditions, use of neuroimaging, EEG, and assessment for neuronal autoantibodies when indicated.[41] The guidelines emphasize the use of standardized assessment tools, such as the Bush-Francis Catatonia Rating Scale (BFCRS), to enhance diagnostic accuracy. In cases of diagnostic uncertainty, a lorazepam challenge test is recommended to confirm the diagnosis. In addition, the guidelines highlight the importance of considering catatonia in various contexts, including mood disorders, psychotic disorders, and general medical conditions.

Diagnosis and Assessment

Timely diagnosis is critical because catatonia is treatable when recognized early. The BFCRS is widely used, though its validation in pediatric populations remains limited. A systematic approach should include:

Validation scales:

• Bush-Francis Catatonia Rating Scale:
• • Sensitivity: 100%
  • Specificity: 88%
  • Description: Gold-standard tool with 23 items assessing catatonic features [25]

The BFCRS comprises 23 items, rated from 0 (absent) to 3 (severe), with the first 14 representing the screening instrument (the Catatonia Screening Instrument) and the full 23 used for detailed severity assessment.[25] 

Other scales:

• Pediatric Catatonia Rating Scale:
• • Sensitivity: 94%
  • Specificity: 89%
  • Description: Adapted for children, better capturing developmental variations [11]
• Kanner Catatonia Rating Scale: Developed to capture catatonic features in autism spectrum disorder, though research on sensitivity and specificity is ongoing [10][42]

Lorazepam challenge test:

The lorazepam challenge test is a rapid bedside assessment that can support a diagnosis of catatonia while simultaneously initiating treatment.[43] A typical adult dose is 2 mg of lorazepam intravenously (lower for frail older adults or those at risk of respiratory depression). Intramuscular or oral routes may be used if intravenous access is unavailable, although they yield slower, less specific responses.[44][45] Clinicians must consider interactions with other medications that can cause or worsen sedation or respiratory depression, such as opioids.[46][47] Clinical improvement can occur within minutes but is commonly assessed over 30 to 120 minutes; some patients require up to 2 to 3 hours for a clear effect.[48][49] If there is no improvement and the patient remains awake with stable vital signs, a second dose is given, with reassessment in 5 to 10 minutes. However, observation can continue for longer periods. A negative response does not exclude catatonia and occurs in approximately 20% or more of patients with catatonia.[49]

Traditional definitions of a positive test result (≥50% reduction on the BFCRS) lack a strong evidence base; meaningful improvement in one or more key symptom domains, such as emergence from mutism to brief speech, may reasonably constitute a positive response. A positive reaction with high pretest suspicion effectively confirms catatonia and justifies scheduled benzodiazepine treatment. A negative or equivocal response with low pretest suspicion argues against catatonia and should prompt evaluation for an alternative diagnosis.

Electroencephalogram, imaging, and cerebral spinal fluid studies:

The primary role of these investigations is to exclude nonconvulsive status epilepticus, encephalitis, and structural lesions.[50] Hosseini et al (2023) conducted a systematic review and meta-analysis evaluating the diagnostic accuracy of EEG in identifying the etiology of catatonia. The study results found that EEG abnormalities were present in 66% of catatonia cases, significantly more common in medical and neurological etiologies (78%) than in primary psychiatric cases (30%). Common EEG findings included diffuse slowing, focal abnormalities, triphasic waves, and patterns indicative of nonconvulsive status epilepticus.

These changes often correlated with underlying conditions such as metabolic encephalopathies, epilepsy, and autoimmune encephalitis. While a normal EEG was frequently observed in psychiatric catatonia, abnormal EEGs were a strong indicator of organic pathology. The study's authors recommend EEG as a standard component of the diagnostic workup for catatonia, particularly in atypical, treatment-resistant, or fluctuating presentations, to improve diagnostic accuracy and clinical outcomes.[50] While an MRI or computed tomography scan cannot directly demonstrate catatonia, brain imaging may reveal abnormalities underlying catatonia. Imaging of other body regions may reveal neoplasms causing paraneoplastic encephalitis.

Other laboratory tests:

Metabolic screens for diseases such as diabetic ketoacidosis, glomerulonephritis, hepatic dysfunction, or other abnormalities may reveal a reversible cause. Inflammatory markers and autoantibody testing may identify autoimmune etiologies of catatonia. 

Vital signs monitoring:

Vital signs should be monitored frequently because autonomic instability may indicate the onset of malignant catatonia, a catatonic syndrome characterized by fever, hypertension, tachycardia, and tachypnea, which can progress to death if not rapidly treated.[36] In summary, in patients with new-onset catatonia, psychiatric causes should be considered first. Still, somatic causes should not be overlooked, particularly when an underlying mental illness does not easily explain the clinical presentation.[51][52]

Treatment / Management

Contemporary guidelines and recent literature emphasize a stepwise, evidence-based approach to the treatment of catatonia.

First-Line Therapy 

Lorazepam, administered orally, often 3 times daily at doses of 4 to 12 mg/d, is typically considered first-line therapy (though different patients respond at different rates).[53][54][55] A clinically meaningful response is often defined as a 50% or more reduction in BFCRS score or rapid partial resolution of core motor signs. A positive lorazepam challenge result supports, but does not definitively confirm, the diagnosis.[41] 

Reported benzodiazepine response rates vary but generally range from 60% to 80%, with greater responsiveness observed in mood disorder–associated catatonia compared with schizophrenia-associated cases.[24][41] Some patients require tapering of lorazepam over several months after symptom control is achieved. Rapid tapering may cause recurrence of catatonic symptoms.[55] Reasonable alternatives to lorazepam are available. Multiple studies' results indicate that oral oxazepam at a 60-mg dose yields therapeutic effects comparable to those achieved with oral lorazepam 2 mg.[56][57] Oral zolpidem at 10 mg has also shown potential benefit.[58][59]

Electroconvulsive Therapy 

Electroconvulsive therapy (ECT) delivers more durable remission for benzodiazepine-refractory or malignant cases, with reported remission rates of approximately 70% to 90% in recent series and guideline reviews.[24][41] When an adequate response to benzodiazepines is not achieved or when rapid control of life-threatening features is required and ECT is unavailable, clinicians may consider second-line or adjunctive pharmacologic strategies. Evidence for these agents derives largely from case series, open-label studies, systematic reviews, and recent guideline statements; randomized controlled data remain sparse for most of the following agents.

NMDA-Modulating Agents (Amantadine, Memantine)

These agents modulate glutamatergic neurotransmission and may correct the excitatory/inhibitory imbalance implicated in catatonia.Results from multiple case reports, series, and narrative reviews describe the benefits of amantadine (100–200 mg/d) or memantine (10–20 mg/d) in benzodiazepine-resistant catatonia. Response is variable and may require several days to weeks before improvement becomes evident.[24][60] Memantine may cause agitation and hallucinations, and renal dose adjustments are necessary in patients with renal impairment.[24][60]

Atypical Antipsychotics (Including Clozapine)

Antipsychotic medications can paradoxically worsen or precipitate catatonia (or neuroleptic malignant syndrome), and are not considered first-line. However, in selected cases, especially when a persistent psychotic disorder underlies catatonia, carefully chosen atypical agents or clozapine have been beneficial. Results from a recent systematic review suggest that clozapine (with strict monitoring for agranulocytosis and myocarditis) may be efficacious in refractory catatonia, though data are observational.[61] Clozapine should be used only after weighing risks and ideally in consultation with specialist teams; slow titration with metabolic and hematologic monitoring per local protocols may be necessary.[24][61]

Mood Stabilizers (Valproate, Lithium)

In catatonia associated with mood disorders, addressing the underlying affective illness with mood stabilizers is frequently employed.[60] Formal trials are lacking; most evidence consists of case reports and small series describing adjunctive valproate or lithium improving catatonic features when mood symptoms predominate or long-term prophylaxis is required. Contemporary guidelines describe mood stabilizers as adjunctive for mood-related catatonia but do not endorse them as primary acute monotherapy.[24][41] Standard therapeutic monitoring (serum drug levels, renal/thyroid function for lithium; hepatic function and platelet counts for valproate) is required.

Ketamine and Esketamine

Intravenous ketamine (commonly 0.5 mg/kg infusion over approximately 40 minutes), in emerging case-series, has shown benefit in some benzodiazepine-refractory catatonia subtypes (especially, retarded catatonia).[62] Use in clinical practice is experimental and should be considered under specialist oversight.[62]

Noninvasive Neuromodulation (Repetitive Transcranial Magnetic Stimulation, Transcranial Direct Current Stimulation)

Results from systematic reviews have reported positive outcomes in refractory catatonia, but heterogeneity and small sample sizes limit the generalizability of recommendations. These modalities may be considered when ECT is contraindicated.[63]

Immunotherapy and Disease-Directed Treatment (Autoimmune and Encephalitic Causes)

When catatonia is secondary to autoimmune encephalitis (eg, anti-NMDA receptor encephalitis), benzodiazepines and ECT may temporarily treat motor and behavioral symptoms, but definitive treatment requires immunotherapy (corticosteroids, intravenous immunoglobulin, plasmapheresis, or rituximab) and oncologic management. Early recognition and simultaneous initiation of immunotherapy are associated with better neurologic outcomes.[23][24]

Differential Diagnosis

The differential diagnosis for catatonia includes the following:

Neuroleptic Malignant Syndrome

• Clinical overlap: Rigidity, fever, autonomic instability, and altered mental status can resemble malignant catatonia.
• Key discriminators: Recent exposure to dopamine-blocking agents is cardinal for neuroleptic malignant syndrome; onset typically occurs over 1 to 3 days after antipsychotic initiation or dose escalation. Marked lead-pipe rigidity, high creatine kinase (often >1000–5000 U/L), and marked leukocytosis are common in neuroleptic malignant syndrome.[64] Catatonia, in contrast, may show waxy flexibility, posturing, or intermittent rigidity rather than uniform lead-pipe tone. Creatine kinase elevations can occur in malignant catatonia but are typically less pronounced.[65]
• Treatment differs: Discontinue dopamine blockers, provide supportive care, and consider dantrolene or bromocriptine. Catatonia responds to benzodiazepines and ECT.[65][66] 

Serotonin Syndrome 

• Clinical overlap: Hyperthermia, agitation, autonomic dysfunction, and altered mental status
• Key discriminators: Hyperreflexia and inducible or spontaneous clonus (especially lower extremity) and recent serotonergic agent exposure (eg, selective serotonin reuptake inhibitors; monoamine oxidase inhibitors; triptans; 3,4-methylenedioxymethamphetamine [MDMA]) are highly suggestive of serotonin syndrome. Onset is typically rapid (within hours). Creatine kinase may be elevated, but usually less marked than NMS. The Hunter Serotonin Toxicity Criteria (clonus ± other features) have high specificity.[67] Catatonia lacks the characteristic hyperreflexia or clonus pattern and usually demonstrates specific motor signs (waxy flexibility, posturing).[68][69]

Akinetic Mutism

• Clinical overlap: There is a profound reduction in spontaneous motor activity and speech.
• Key discriminators: Akinetic mutism is typically due to frontal lobe or mesencephalic lesions (stroke, tumor). Patients have preserved wakefulness and motor capacity but cannot initiate speech or movement. Eye tracking and spontaneous visual pursuit may be preserved. Neuroimaging (MRI/CT) commonly reveals focal lesions.[70] EEG often shows background slowing consistent with structural or metabolic injury.[50] Akinetic mutism lacks behavioral signs of catatonia such as echophenomena, negativism, and automatic obedience, and usually does not improve with lorazepam.[70][71]
• Evaluation: MRI and careful bedside assessment of eye movements and volition.[71]

 Malignant Hyperthermia 

• Clinical overlap: This includes hyperthermia, rigidity, autonomic instability, and elevated creatine kinase levels.
• Key discriminators: Malignant hyperthermia occurs in the perianesthetic setting after exposure to volatile anesthetic agents or succinylcholine and features abrupt hypercapnia, acidosis, and severe hyperthermia. Genetic predisposition is associated with mutations in RYR1 and CACNA1S. Time course and triggering exposure distinguish malignant hyperthermia from catatonia.
• Laboratory hallmarks: Rapid, extreme creatine kinase level elevation, hyperkalemia, and mixed respiratory and metabolic acidosis
• Management: Dantrolene administration and anesthetic cessation [72]

Locked-In Syndrome 

• Clinical overlap: Apparent immobility and mutism
• Key discriminators: Locked-in syndrome typically results from ventral pontine injury (ischemic or hemorrhagic), producing quadriplegia and anarthria but with preserved consciousness and vertical eye movements or blinking. Patients can communicate via these vertical eye movements. MRI shows a brainstem lesion; EEG and cognition are largely preserved. Please see StatPearls' companion resource, "Locked-in Syndrome," for further information.

Stiff Person Spectrum Disorders 

• Clinical overlap: Marked axial or truncal stiffness and freezing gait that can mimic retarded catatonia
• Key discriminators of the Stiff person spectrum include painful episodic spasms, progressive stiffness of axial muscles, and electromyographic evidence of continuous motor unit activity at rest. Serum anti-GAD65 or anti-glycine receptor antibodies are often present. Stimuli trigger symptoms and are often painful; cognition is preserved. Stiff person spectrum responds to immunotherapy, benzodiazepines, and other symptomatic agents.[73]

Parkinson Disease

• Clinical overlap: Bradykinesia, rigidity, reduced spontaneous movement
• Key discriminators: Parkinson disease presents with rest tremor, bradykinesia with asymmetric onset, postural instability, and usually a slow, chronic, progressive course. A robust levodopa response supports the diagnosis of Parkinson disease.[74][75]

Stroke

• Clinical overlap: Sudden immobility, mutism, or focal motor deficits
• Key discriminators: Stroke produces focal neurologic deficits localized to vascular territories; brain imaging (CT or MRI with diffusion-weighted imaging) usually demonstrates ischemia or hemorrhage. Onset is typically abrupt. Catatonia, in contrast, is often global and behavioral, with characteristic motor signs, and is not confined to a vascular distribution.[76][77]

Delirium and Dementia

• Clinical overlap: Reduced responsiveness, abnormal motor behavior, altered cognition, or attention
• Key discriminators: Delirium is characterized by an acute onset, fluctuating course, and impaired attention and awareness; EEG typically shows generalized slowing. Dementia presents with progressive cognitive decline over months or years.[65]

Elective or Selective Mutism (Volitional Mutism)

• Clinical overlap: Mutism
• Key discriminators: Selective or elective mutism is behavioral and context-dependent (child speaks in some settings but not others), with preserved nonverbal communication and no motor signs of catatonia. Neurologic examination and EEG findings are normal, and there are no other signs of catatonia.

Anti-NMDA Receptor Encephalitis (and Other Autoimmune Encephalitides)

• Clinical overlap: Acute psychiatric syndrome with prominent motor phenomena (stupor, mutism, orofacial dyskinesias) and autonomic dysfunction that can present with a catatonic picture.
• Key discriminators: Younger age, rapid progression of behavioral/psychotic features, seizures, orofacial dyskinesias, autonomic instability, and decreased consciousness are characteristic. Cerebrospinal fluid findings include pleocytosis, oligoclonal bands, or NMDA receptor antibodies in cerebrospinal fluid or serum, and a characteristic EEG, "extreme delta brush" pattern, strongly indicates anti-NMDA encephalitis.[50][78][79] Immunotherapy (intravenous immunoglobulin, corticosteroids, plasmapheresis, rituximab) is indicated, distinct from primary catatonia management.[79]

Prognosis

The prognosis of catatonia is generally favorable with timely recognition and appropriate treatment, particularly with benzodiazepines and ECT, which often produce rapid and dramatic responses.[65] Delayed diagnosis, however, increases the risk of progression to malignant catatonia, medical complications, or chronic disability.[65] Mortality in malignant catatonia remains significant if the disease is left untreated, though early intervention reduces fatal outcomes substantially.[80][81] Prognosis also depends on etiology: mood disorder–related catatonia responds best,[82] whereas schizophrenia-associated and autoimmune-related catatonias may require prolonged or multimodal interventions.[79][82]

Complications

Catatonia, though a treatable neuropsychiatric syndrome, poses serious risks when unrecognized or inadequately treated. The complications span medical, psychiatric, and iatrogenic domains, with the severity escalating in malignant or prolonged forms. Medically, untreated catatonia can lead to dehydration, malnutrition, aspiration pneumonia, urinary retention, pressure ulcers, venous thromboembolism, and life-threatening autonomic instability, particularly in malignant catatonia, when hyperthermia, tachycardia, and rigidity resemble neuroleptic malignant syndrome.[64] Prolonged immobility increases the risk of rhabdomyolysis and multiorgan dysfunction. Psychiatrically, delayed treatment may worsen mood or psychotic symptoms, cognitive decline, and chronic disability.

In children and adolescents, regression in developmental functioning, especially in those with autism spectrum disorder, can become irreversible without early intervention. Diagnostic overshadowing, especially in autism spectrum disorder or severe mood disorders, may result in misattribution of symptoms, delaying targeted therapy. Iatrogenic harm may also occur when antipsychotics are inappropriately administered, exacerbating catatonia or precipitating malignant deterioration. Furthermore, the underuse of ECT due to stigma or systemic barriers limits access to this potentially life-saving intervention. Overall, catatonia demands prompt identification and interdisciplinary coordination, as the window for effective reversal is narrow, and complications significantly elevate morbidity and mortality across all age groups.[16][24]

Deterrence and Patient Education

Deterrence of catatonia complications relies on early detection, judicious medication use, and widespread clinical awareness, while patient and family education fosters understanding, reduces stigma, and enhances treatment compliance. A collaborative approach, across psychiatry, neurology, pediatrics, and nursing, is critical to minimize morbidity and empower families in the ongoing care of affected individuals. Early identification and intervention significantly reduce the risk of severe complications such as autonomic instability, rhabdomyolysis, or progression to malignant catatonia. Therefore, empowering patients, families, and caregivers with knowledge is a key component of care.

Deterrence Strategies

• Routine screening in high-risk populations: Regular monitoring for catatonic symptoms is advised in populations at elevated risk, such as individuals with autism spectrum disorder, mood disorders, and recent exposure to antipsychotic medications. Incorporating structured tools like the BFCRS or the Pediatric Catatonia Rating Scale into routine psychiatric assessments facilitates early detection.
• Cautious use of antipsychotics: Antipsychotics should be used judiciously, especially in patients presenting with unexplained immobility, mutism, or stupor. Inappropriate use may precipitate or worsen catatonia and induce neuroleptic malignant syndrome.
• Education of healthcare providers: Interprofessional training initiatives should ensure that clinicians across disciplines can recognize varied presentations. The British Association for Psychopharmacology guidelines emphasize this interdisciplinary awareness as essential to deterrence.
• Prompt intervention protocols: Hospitals and psychiatric units should implement clear, protocol-driven responses, including access to lorazepam challenge testing and early consideration of ECT for refractory cases.

  Patient and Family Education

• Understanding catatonia: Informing patients and their families that catatonia is a treatable medical condition, rather than a manifestation of laziness, willful behavior, or a strictly psychiatric illness. Describing it as a brain-based syndrome involving disruptions in motor and emotional regulation can reduce stigma.
• Recognizing symptoms: Families should be taught to watch for signs such as mutism, immobility, waxy flexibility, echolalia, agitation, and abnormal posturing, particularly when these symptoms occur in conjunction with mood symptoms, psychosis, or abrupt behavioral regression.
• Importance of timely care: Education should emphasize that early treatment with benzodiazepines or ECT can be life-saving and significantly reduce long-term complications. Delays increase the likelihood of hospitalization, cognitive decline, or progression to malignant catatonia.
• Treatment expectations: Families should understand that lorazepam often leads to rapid symptom relief, but ongoing treatment may include maintenance benzodiazepines, ECT, or immunotherapy (in cases of autoimmune disease, such as anti-NMDA receptor encephalitis).
• Reducing relapse risk: After remission, families should be counseled on monitoring for recurrence, particularly in individuals with mood disorders or those with a prior catatonic episode. Treatment adherence and regular psychiatric follow-up are essential.
• Addressing cultural and systemic barriers: Misconceptions about ECT or psychiatric care in general must be addressed compassionately, using culturally competent communication. Normalizing these treatments as safe, evidence-based, and often critical to recovery is essential for building trust.

Enhancing Healthcare Team Outcomes

Catatonia is a complex, often misunderstood neuropsychiatric syndrome characterized by a range of psychomotor disturbances, including stupor, mutism, echolalia, posturing, and agitation. Catatonia can occur across the lifespan and is associated with various underlying psychiatric, neurologic, autoimmune, and medical conditions. Despite being highly treatable, particularly with benzodiazepines and ECT, delayed diagnosis remains common, increasing the risk of life-threatening complications such as malignant catatonia, rhabdomyolysis, and autonomic instability. Updated consensus guidelines and growing research underscore the need for early recognition, appropriate use of diagnostic tools, and tailored treatment approaches. Pediatric populations and those with developmental disorders, such as autism spectrum disorder, present unique diagnostic and management challenges, further necessitating a collaborative, interdisciplinary response.[83][84]

Interprofessional Team Collaboration

Optimal outcomes in catatonia care require seamless coordination among psychiatrists, pediatricians, neurologists, nurses, pharmacists, social workers, and rehabilitation specialists. Interprofessional teams must communicate openly, strategize proactively, and create shared care pathways to reduce delays and prevent complications. The Joint Accreditation’s emphasis on flattening healthcare hierarchies is exemplified in catatonia management, where each team member’s insight enhances diagnostic accuracy and therapeutic outcomes. Interprofessional continuing education fosters this unity, promoting a culture of collaborative, patient-centered care.

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Disclosure: Veeraraghavan Iyer declares no relevant financial relationships with ineligible companies.

Disclosure: Benjamin Spurling declares no relevant financial relationships with ineligible companies.

Disclosure: Abid Rizvi declares no relevant financial relationships with ineligible companies.